The BMP antagonist noggin regulates cranial suture fusion

@article{Warren2003TheBA,
  title={The BMP antagonist noggin regulates cranial suture fusion},
  author={Stephen M. Warren and Lisa J. Brunet and Richard M. Harland and Aris N. Economides and Michael T. Longaker},
  journal={Nature},
  year={2003},
  volume={422},
  pages={625-629}
}
During skull development, the cranial connective tissue framework undergoes intramembranous ossification to form skull bones (calvaria). As the calvarial bones advance to envelop the brain, fibrous sutures form between the calvarial plates. Expansion of the brain is coupled with calvarial growth through a series of tissue interactions within the cranial suture complex. Craniosynostosis, or premature cranial suture fusion, results in an abnormal skull shape, blindness and mental retardation… 
Augmentation of smad‐dependent BMP signaling in neural crest cells causes craniosynostosis in mice
  • Y. Komatsu, P. Yu, Y. Mishina
  • Medicine, Biology
    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
  • 2013
TLDR
It is shown that enhanced bone morphogenetic protein (BMP) signaling through the BMP type IA receptor (BMPR1A) in cranial neural crest cells, but not in osteoblasts, causes premature suture fusion in mice, suggesting an important contribution of dysregulated BMP signaling to syndromic craniosynostoses and potential strategies for early intervention.
Gnas Loss Causes Chondrocyte Fate Conversion in Cranial Suture Formation
TLDR
The role of Gαs in maintaining cranial chondrocyte identity during neonatal calvaria development in mice is uncovered and how reduction of Hh signaling could be a nonsurgical intervention to reduce skull deformity in craniosynostosis due to loss of GNAS is uncovered.
Regulation of Cranial Suture Morphogenesis
TLDR
Significant delay in the timing of suture fusion and increases in the expression domains of FGFR1 and 2 were observed, demonstrating the sensitivity of sutures patency to mechanical signals and a possible role of the FGF system in mediating such stimuli.
The BMP Ligand Gdf6 Prevents Differentiation of Coronal Suture Mesenchyme in Early Cranial Development
TLDR
Although BMPs are known to promote bone formation, Gdf6 plays an inhibitory role to prevent the osteogenic differentiation of the coronal suture mesenchyme, prior to the onset of calvarial ossification.
Regulation of Craniofacial Bone Healing Using Noggin
TLDR
The work presented here demonstrates that a single dose of Noggin protein is capable of inhibiting resynostosis and improving craniofacial growth after surgery to correct craniosynostotic in rabbits.
The Balance of WNT and FGF Signaling Influences Mesenchymal Stem Cell Fate During Skeletal Development
TLDR
Endochondral ossification is identified as a mechanism of suture closure during development and implicates this process in craniosynostosis, a developmental disorder resulting from premature closure of the gaps between skull bones.
Medical treatment of craniosynostosis: recombinant Noggin inhibits coronal suture closure in the rat craniosynostosis model.
TLDR
The chimeric nude rate model is a viable model of craniosynostosis and the addition of rhNoggin to prematurely fusing sutures should prevent synostosis, demonstrating one of the mechanisms for premature suture fusion.
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